Ryegrasses (genus Lolium) are commonly used to feed animals throughout the world. Such grasses can often be infected with endophyte fungi, such as those from the Neotyphodium genus. These fungi can live on these grasses and produce compounds (such as alkaloids) which can be useful to the plant. Some of these compounds can also be harmful to animals that consume the infected plant, and result in toxicosis.
One such example is the toxicosis resulting from the fungus Neotyphodium lolii, which produces the alkaloid lolitrem B in perennial ryegrass (Lolium perenne). This toxin forms a major component of the toxicosis called perennial ryegrass toxicosis (PRGT), or “Ryegrass Staggers”, and can lead to neuromuscular dysfunction with symptoms such as tremors, staggers, ataxia, hyperaesthesia, tetany, gait abnormalities, increased severity of ill-coordination on movement and initial or continued sternal recumbency. These effects can be further exacerbated by external stimuli, and severe forms can lead to death of the animal, typically as a result of dehydration, starvation or attack by predators. Milder effects of lolitrem B-induced toxicosis can also have severe commercial outcomes, such as reduced live-weight gain, scouring and increased DAG formation, reduced fertility and low milk yields. The toxicoses that affect ruminants grazing Phalaris also cause tremors and other neurological and systemic clinical signs to those observed in respect of PRGT.
There is currently no known cure for treating animals with lolitrem B intoxication, PRGT or Phalaris toxicosis and the subsequent animal morbidity and mortality impacts adversely on animal welfare and results in enormous losses in animal production revenue. Animals may recover from such conditions if they can be moved away from the infected pastures. However, this is not always possible, especially where large pasture areas are infected and many animals are grazing on that pasture.
Whilst endophyte-infected pastures can be removed and replaced with grass that is not infected, this is of great effort and cost to achieve and is not always successful. The replacement grass may also not be as viable as the endophyte-infected pasture because it may be more prone, for example, to drought, due to the loss of the protective effects that the endophytes provide to the plants. Similarly, it is difficult to ensure that the endophyte infected seed is completely removed from the pasture, which may result in re-infection. Removal and replacement of endophyte-infected pastures is therefore not always performed.
It is also difficult and time-consuming to test for the endophytes. Testing can only be performed by laboratory analysis, and representative samples taken from a large spread of the pasture need to be carefully collected and tested within a short time frame. Testing is therefore not always practical and may not be accurate depending on factors such as the samples selected and submitted, and the transportation conditions of the samples to the laboratory.
There have been several other approaches investigated to overcome the problems of endophyte-induced toxicosis. A grass modified to be unfavourable to endophyte infection may overcome the problem of pasture re-infection. However, similarly to the replacement pastures, as the endophytes also provide the plant with benefits such as resistance to drought and protection from insects, this approach can still greatly disadvantage the plant and viability of the pastures.
Another approach has been to investigate the selective breeding or genetic modification of the endophyte to maximise its positive effects on the plant (e g insecticide properties) whilst minimising the expression of the toxicosis-causing alkaloids. These approaches, however, are expensive and have been shown to be not completely effective and/or commercially practical across all levels of farming.
Another approach includes feeding animals additives to overcome the toxicity of the alkaloids. An example of this is outlined in patent application WO 00/65928, whereby a modified yeast cell wall and a mineral clay is fed to animals to inactivate the ergot alkaloids causing fescue toxicosis, by binding the alkaloids within the gastrointestinal tract (before their systemic absorption). This treatment does not interfere with the pharmacodynamics of the endophytic alkaloid, but prevents its absorption. As such, this approach does not treat the symptoms of fescue toxicosis, but can minimise the effect of the alkaloids on the animal.
Whilst these approaches have each displayed some success, none have been able to significantly reduce the impact of alkaloid-induced toxicosis using a practical, commercially viable technique.
Reference to any prior art in the specification is not an acknowledgment or suggestion that this prior art forms part of the common general knowledge in any jurisdiction or that this prior art could reasonably be expected to be understood, regarded as relevant, and/or combined with other pieces of prior art by a skilled person in the art.